Fulminant eosinophilic myocarditis treated by venoarterial extracorporeal membrane oxygenation and adjunctive...

Eosinophilic myocarditis can result from drug hypersensitivity or various systemic disorders. Although corticosteroids are effective, treatment strategies are not standardized.

A 78-year-old male presented with dyspnoea. On admission, he was febrile and hypotensive and had sinus tachycardia with a newly developed right bundle branch block. Laboratory findings showed marked eosinophilia with elevated troponin. The patient rapidly progressed to cardiogenic shock, and venoarterial extracorporeal membrane oxygenation (VA-ECMO) was applied. Eosinophilic myocarditis was suspected, and endomyocardial biopsy confirmed dense myocardial eosinophil infiltration consistent with the diagnosis. Review of history revealed recent cefaclor use for a hand injury as the probable cause. The patient's condition quickly improved after initiation of high-dose intravenous methylprednisolone, allowing weaning from VA-ECMO. However, persistent troponin elevation and myocardial inflammation on fluorodeoxyglucose positron emission tomography (FDG-PET) were observed despite 5 weeks of steroid therapy. Subcutaneous mepolizumab, an anti-interleukin-5 monoclonal antibody, was initiated as an adjunctive immunosuppressive therapy. After seven cycles, troponin levels normalized, cardiac function fully recovered, and follow-up FDG-PET demonstrated a marked reduction in myocardial inflammation.

We describe a case of fulminant eosinophilic myocarditis that was possibly associated with cefaclor use and successfully managed with VA-ECMO and adjunctive immunosuppressive therapy. Fluorodeoxyglucose positron emission tomography imaging helped detect residual inflammation and assess treatment response. Immunosuppressive therapy allowed a reduction of steroid dose, mitigating the risk of steroid-related side effects.